mangostin and Liver-Failure--Acute

The purpose of this study was to investigate the hepatoprotective effect of α-mangostin (α-MG) on lipopolysaccharide/d-galactosamine (LPS/D-GalN)-induced acute liver failure and discover its potential mechanisms in mice. The results showed that α-MG could attenuate LPS/D-GalN-induced liver pathological injury, and decrease the hepatic malondialdehyde (MDA) level, serum alanine aminotransferase (ALT), aspartate transaminase (AST), tumor necrosis factor (TNF-α), interleukin-1β and 6 (IL-1β, IL-6) levels and recovery hepatic glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) activities. The results also indicated that α-MG inhibited LPS/D-GalN-induced toll-like receptor 4 (TLR4) expression and NF-κB activation. In addition, α-MG up-regulated the expressions of Nrf2 and heme oxygenase-1 (HO-1). In conclusion, the results indicated that α-MG could protect against LPS/D-GalN-induced liver failure by activating Nrf2 to induce antioxidant defense and inhibiting TLR4 signaling pathway to induce anti-inflammatory effect.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Biomarkers; Chemical and Drug Induced Liver Injury; Cytoprotection; Disease Models, Animal; Dose-Response Relationship, Drug; Galactosamine; Heme Oxygenase-1; Lipopolysaccharides; Liver; Liver Failure, Acute; Male; Membrane Proteins; Mice, Inbred ICR; NF-E2-Related Factor 2; Oxidative Stress; Signal Transduction; Toll-Like Receptor 4; Xanthones